2021
DOI: 10.1016/j.jid.2020.09.019
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ACE2 Expression on the Keratinocytes and SARS-CoV-2 Percutaneous Transmission: Are they Related?

Abstract: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, a… Show more

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Cited by 5 publications
(4 citation statements)
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“…While exogenous Ace2 expression is sufficient to render cells competent for SARS-Cov-2 infection 3 , tissue expression of Ace2 is not always an indicator of viral tropism 4 . A case in point is the skin that expresses Ace2 in the epidermis in-vivo 5 , and keratinocytes in-vitro (Fig S1A) but nevertheless is not considered as a primary route of infection 6 . In support of this, exposure of human epidermal keratinocytes to SARS-CoV-2 does not result in a productive infection (Fig S1B).…”
Section: Figurementioning
confidence: 99%
“…While exogenous Ace2 expression is sufficient to render cells competent for SARS-Cov-2 infection 3 , tissue expression of Ace2 is not always an indicator of viral tropism 4 . A case in point is the skin that expresses Ace2 in the epidermis in-vivo 5 , and keratinocytes in-vitro (Fig S1A) but nevertheless is not considered as a primary route of infection 6 . In support of this, exposure of human epidermal keratinocytes to SARS-CoV-2 does not result in a productive infection (Fig S1B).…”
Section: Figurementioning
confidence: 99%
“…En la piel, la expresión de ECA-2 es mayor en los queratinocitos en comparación con las células de las glándulas sudoríparas, los fibroblastos y los melanocitos (18,19) . Hasta el momento, no se ha establecido la transmisión percutánea del virus (19)(20)(21) .…”
Section: Mecanismos Fisiopatológicosunclassified
“…El virus podría desencadenar apoptosis de las células que invade; a nivel del endotelio vascular, causa daño inflamatorio directo sobre las células, que progresa a microangiopatía sistémica y coagulación intravascular diseminada (CID) en casos severos, lo que sugiere que esta condición sea una vasculitis viral generalizada con manifestaciones cutáneas (14,16,24) . En los linfocitos T, promueve su apoptosis, lo que genera linfopenia, alteración de la respuesta inmunitaria adaptativa e infección descontrolada (17,21,25) . La replicación inicial del virus en las células epiteliales conduciría a su propagación hematógena, con exposición de fragmentos de la cápside viral al complejo mayor de histocompatibilidad tipo I, que activaría los linfocitos T CD8 + (24) .…”
Section: Mecanismos Fisiopatológicosunclassified
“…While exogenous ACE2 expression is sufficient to render cells competent for SARS-CoV-2 infection (3), tissue expression of ACE2 is not always an indicator of viral tropism (4). A case in point is the skin, which expresses ACE2 in the epidermis in-vivo (5), and keratinocytes in-vitro (Figures 1A, S1A) but nevertheless, it is not considered as a primary route of infection (6). In support of this, exposure of human epidermal keratinocytes to SARS-CoV-2 does not result in a productive infection (Figure 1B).…”
Section: Introductionmentioning
confidence: 99%